Neurocognitive functioning and health-related quality of life in patients with radiologically suspected meningiomas.

Few data are available concerning the neurocognitive outcome and health-related quality of life (HRQOL) following neurosurgery in meningioma patients, and even less is known about neurocognitive functioning and HRQOL in untreated patients with stable lesions. The present study aims at quantifying the nature and extent of neurocognitive deficits and HRQOL in suspected WHO grade I meningioma patients who have not received surgery and/or radiotherapy and compare outcome to that of healthy controls. Neurocognitive functioning was assessed by using a standardized test battery in 21 radiologically suspected WHO grade I meningioma patients with a wait-and-scan approach. HRQOL was assessed with the MOS SF-36 questionnaire. These patients were matched for age, sex, and education with 21 healthy controls. Associations between neurocognitive functioning on the one hand and HRQOL and tumor characteristics on the other were determined. Compared to healthy controls, meningioma patients had lower psychomotor speed (p = 0.011) and working memory capacity (p = 0.034) and furthermore attained lower levels of self-perceived general health and vitality. Neurocognitive functioning in untreated patients was not related to tumor volume, edema or tumor lateralization. No correlations were found between psychomotor speed or working memory and HRQOL. Untreated meningioma patients with stable lesions have limitations in neurocognitive functioning and HRQOL. In deciding upon a treatment strategy these reductions in functioning should be taken into consideration and communicated with the patient.

Late neurocognitive sequelae in patients with WHO grade I meningioma.

BACKGROUND: Information on neurocognitive outcome following treatment of benign meningiomas is virtually lacking. This is remarkable considering that survival in these patients is the most favourable of all intracranial tumours. The aim of the present study was therefore to document the extent and nature of neurocognitive deficits in patients with World Health Organization (WHO) grade I meningioma after treatment. METHODS: 89 patients with WHO grade I meningioma who underwent surgery with or without adjuvant radiotherapy were individually matched to 89 healthy controls for age, sex and educational level. Neurocognitive functioning of patients was assessed at least 1 year following treatment and compared with that of healthy controls using the Student's t test. Additionally, associations between tumour characteristics (size, lateralisation and localisation), treatment characteristics (radiotherapy) and epilepsy burden (based on seizure frequency and antiepileptic drug use) and neurocognitive functioning were investigated. RESULTS: Compared with healthy controls, patients with meningioma showed significant impairments in executive functioning (p<0.001), verbal memory (p<0.001), information processing capacity (p = 0.001), psychomotor speed (p = 0.001) and working memory (p = 0.006). Patients with skull base meningiomas performed significantly lower on three out of six neurocognitive domains compared with convexity meningiomas. Left-sided as opposed to right-sided meningiomas were related to verbal memory deficits. A higher epilepsy burden was significantly associated with lower executive functioning which primarily could be attributed to antiepileptic drug use. No significant associations were established between neurocognitive status and radiotherapy or tumour volume. CONCLUSIONS: Meningioma patients are characterised by long term deficits in neurocognitive functioning that can partly be attributed to the use of antiepileptic drugs and tumour location but not to the use of radiotherapy.

Genetics and pharmacogenomics of diffuse gliomas.

Rapidly evolving techniques for analysis of the genome provide new opportunities for cancer therapy. For diffuse gliomas this has resulted in molecular markers with potential for personalized therapy. Some drugs that utilize pharmacogenomics are currently being tested in clinical trials. In melanoma, lung-, breast-, gastric- and colorectal carcinoma several molecular markers are already being clinically implemented for diagnosis and treatment. These insights can serve as a background for the promise and limitations that pharmacogenomics has for diffuse gliomas. Better molecular characterization of diffuse gliomas, including analysis of the molecular underpinnings of drug efficacy in clinical trials, is urgently needed. We foresee exciting developments in the upcoming years with clinical benefit for the patients.